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Category: life extension – Page 47
OneSkin, founded by Brazilian PhD scientists in 2016, reports that it has now closed a Series A funding round led by Selva Ventures, together with contributions from PLUS Capital, Unilever Ventures, Able Partners, SOSV, and Meta Planet. This brings the accumulated capital of the firm to 20 million US dollars.
The goal of the OneSkin team is the research and development of topical treatments that promote skin longevity. The brand’s efforts have led to the development of the peptide OS-01, which is claimed to reverse the aging of the skin by preventing the accumulation of “old”, non-dividing senescent cells, as well as shield skin cells from DNA damage. OS-01 is already available on the market in several different products offered by the company.
Senescent cells have been the focus of a significant amount of biogerontological research in recent years. Scientists claim that every cell in the human body has a limited capacity for division, governed by genetic factors. When the cells reach the point in their lifecycle where their ability to divide is permanently halted, they remain in a minimally-functional state in the tissue types they inhabit.
Skull bone marrow expands during adult life, exhibits lifelong vascular growth and increases its haematopoietic potential during ageing.
Summary: Adolescents are known for making less optimal, noisy decisions, but a recent study reveals that these tendencies decrease with age and are linked to improvements in complex decision-making skills. Researchers found that decision noise, or variability in choices, mediates age-related gains in goal-directed behaviors and adaptability.
Adolescents may rely on less efficient strategies due to limited cognitive resources, which makes them more susceptible to emotional and motivational influences. These findings shed light on the computational mechanisms behind developmental shifts in decision-making and open avenues for understanding neurodevelopmental disorders.
Researchers from Johns Hopkins University have recently discovered several prominent biomarkers that allow for the early diagnosis of dementia and/or mild cognitive impairment (MCI). In a recently published article, evidence has been presented that patients with diabetes type 2 exhibited more changes to their brains than healthy controls, including the shrinking of certain brain areas. These changes occurred earlier in life, and some of the patients developed MCI sooner than others.
The Older Controls at Risk for Dementia (BIOCARD) study is a long-term trial which has been conducted for the past 27 years with the goal of determining how medical conditions and other factors might be impacting cognitive function and perhaps even affecting the biological age of the brain as a whole. BIOCARD was originally a National Institutes of Health initiative, which began in 1995 and later continued at Johns Hopkins University from 2015 to 2023. The cohort consisted of 185 participants, with an average age of 55 years and normal cognitive function.
The trial subjects received routine brain scans and cerebrospinal fluid (CSF) tests for 20 years, in order to measure changes in brain structures and levels of proteins associated with Alzheimer’s disease. Scientists have been increasingly using CSF to attempt to uncover early signs of neurodegenerative disease, since it is a minimally-invasive procedure which is inexpensive and widely available.
Aging is characterized by a gradual decline in function, partly due to accumulated molecular damage. Human skin undergoes both chronological aging and environmental degradation, particularly UV-induced photoaging. Detrimental structural and physiological changes caused by aging include epidermal thinning due to stem cell depletion and dermal atrophy associated with decreased collagen production. Here, we present a comprehensive single-cell atlas of skin aging, analyzing samples from young, middle-aged, and elderly individuals, including both sun-exposed and sun-protected areas. This atlas reveals age-related cellular composition and function changes across various skin cell types, including epidermal stem cells, fibroblasts, hair follicles, and endothelial cells. Using our atlas, we have identified basal stem cells as a highly variable population across aging, more so than other skin cell populations such as fibroblasts. In basal stem cells, we identified ATF3 as a novel regulator of skin aging. ATF3 is a transcriptional factor for genes involved in the aging process, with its expression reduced by 20% during aging. Based on this discovery, we have developed an innovative mRNA-based treatment to mitigate the effects of skin aging. Cell senescence decreased 25% in skin cells treated with ATF3 mRNA, and we observed an over 20% increase in proliferation in treated basal stem cells. Importantly, we also found crosstalk between keratinocytes and fibroblasts as a critical component of therapeutic interventions, with ATF3 rescue of basal cells significantly enhancing fibroblast collagen production by approximately 200%. We conclude that ATF3-targeted mRNA treatment effectively reverses the effects of skin aging by modulating specific cellular mechanisms, offering a novel, targeted approach to human skin rejuvenation.
The authors have declared no competing interest.
Johns Hopkins University-led researchers, working with the Biomarkers for Older Controls at Risk for Dementia (BIOCARD) cohort, have found that certain factors are linked to faster brain shrinkage and quicker progression from normal thinking abilities to mild cognitive impairment (MCI). People with type 2 diabetes and low levels of specific proteins in their cerebrospinal fluid showed more rapid brain changes and developed MCI sooner than others.
Long-term studies tracking brain changes over many years are rare but valuable. Previous research mostly provided snapshots in time, which can’t show how individual brains change over the years. By following participants for up to 27 years (20-year median), this study offers new insights into how health conditions might speed up brain aging.
In a study, “Acceleration of Brain Atrophy and Progression From Normal Cognition to Mild Cognitive Impairment,” published in JAMA Network Open, researchers used the BIOCARD cohort to examine risk factors associated with the acceleration of brain atrophy and progression from normal cognition to MCI. An Invited Commentary is also available.
For most animals, ageing is a one-way journey. In a recent PNAS publication, researchers Joan Soto-Angel and Pawel Burkhardt discovered that a species of comb jelly can reverse its life cycle, returning from adulthood to a larval stage.
As people who research aging like to quip, the best thing you can do to increase how long you live is to pick good parents. After all, it has long been recognized that longer-lived people tend to have longer-lived parents and grandparents, suggesting that genetics influence longevity.
Complicating the picture, however, is that we know that the sum of your lifestyle, specifically diet and exercise, also significantly influences your health into older age and how long you live. What contribution lifestyle versus genetics makes is an open question that a recent study in Nature has shed new light on.
Scientists have long known that reducing calorie intake can make animals live longer. In the 1930s, it was noted that rats fed reduced calories lived longer than rats who could eat as much as they wanted. Similarly, people who are more physically active tend to live longer. But specifically linking single genes to longevity was until recently a controversial one.
